Melatonin: Therapeutic Intervention in Mild Cognitive Impairment and Alzheimer Disease

Grandy, John K.

doi:10.4172/2155-9562.1000148

Cited by 9 publications

(7 citation statements)

References 31 publications

(31 reference statements)

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“…The presence of the apolipoprotein E-ε4/4 genetic allele has been associated with decreases in melatonin, and this variant allele is strongly correlated with the development of AD (Liu et al, 1999;Grandy, 2013). This and several other genetic and epigenetic defects (Cacabelos et al, 2015) so far identified in dementias allude to the important roles played by genes in the aetiopathogenesis of the disease, as well their possible role in the development of new therapeutic strategies.…”

Section: Melatonin's Possible Role In Gene-therapy For Dementiamentioning

confidence: 96%

Melatonin and Major Neurocognitive Disorders: Beyond the Management of Sleep and Circadian Rhythm Dysfunction

Onaolapo¹,

Onaolapo²

2018

Sleep Hypn

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Major neurocognitive disorders (dementias) are characterised by impairments in memory, cognition, and several aspects of behaviour. Sleep disorders arising from circadian rhythm and sleep-wake cycle dysfunctions are among the most-troubling challenges encountered in individuals with dementia; and for which administration of melatonergic agents is an important management option. However, in addition to this, melatonin and melatonin receptor agonists appear unique in their potential for modulating symptoms known to be associated with major neurocognitive disorders, or altering the course of the underlying pathology. Hence, they are being continuously investigated for their ability to prevent or reverse cognitive decline, as well as for their antioxidant/neuroprotective properties. In this review, we examine the roles of melatonin and melatonergic agents in the management of major neurocognitive disorders, by looking beyond their classic roles in the management of dementiarelated sleep disorders, to other potential roles in the overall management of symptoms and improvement of the quality of life of individuals with dementia.

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Section: Melatonin's Possible Role In Gene-therapy For Dementiamentioning

confidence: 96%

Melatonin and Major Neurocognitive Disorders: Beyond the Management of Sleep and Circadian Rhythm Dysfunction

Onaolapo¹,

Onaolapo²

2018

Sleep Hypn

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“…Decreased levels of melatonin in serum and in cerebrospinal fluid (CSF), are observed in patients with AD. Melatonin is a hormone that regulates sleep-wake cycles and as the individual ages or in some age-related diseases, the endogenous secretion of melatonin drops markedly, and melatonin supplementation can ameliorate sleep disorders [ 118 ].…”

Section: Molecular Hybrids Designed As Prototypes Of Drug Candidates mentioning

confidence: 99%

Molecular Hybridization as a Tool in the Design of Multi-target Directed Drug Candidates for Neurodegenerative Diseases

Gontijo

Viegas

Ortiz

et al. 2020

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Neurodegenerative Diseases (NDs) are progressive multifactorial neurological pathologies related to neuronal impairment and functional loss from different brain regions. Currently, no effective treatments are available for any NDs, and this lack of efficacy has been attributed to the multitude of interconnected factors involved in their pathophysiology. In the last two decades, a new approach for the rational design of new drug candidates, also called multitarget-directed ligands (MTDLs) strategy, has emerged and has been used in the design and for the development of a variety of hybrid compounds capable to act simultaneously in diverse biological targets. Based on the polypharmacology concept, this new paradigm has been thought as a more secure and effective way for modulating concomitantly two or more biochemical pathways responsible for the onset and progress of NDs, trying to overcome low therapeutical effectiveness. As a complement to our previous review article (Curr. Med. Chem. 2007, 14 (17), 1829-1852. https://doi.org/10.2174/092986707781058805), herein we aimed to cover the period from 2008 to 2019 and highlight the most recent advances of the exploitation of Molecular Hybridization (MH) as a tool in the rational design of innovative multifunctional drug candidate prototypes for the treatment of NDs, specially focused on AD, PD, HD and ALS.

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“…However, while increased plasma levels of sTNF-R1 were associated with memory functions in healthy individuals [ 17 ], the putative links between sTNF-R1 and cognitive performance, as well as structural brain changes in predementia subjects, remain unclear. Within the spectrum of cognitive impairment and dementia, predementia (which may include MCI or cognitive impairment, no dementia (CIND)) represents a clinically important stage when disease-modifying interventions may still be possible [ 18 , 19 ]. Furthermore, associations between sTNF-R1 and neuroimaging features of CSVD await investigation.…”

Section: Introductionmentioning

confidence: 99%

Elevated Soluble TNF-Receptor 1 in the Serum of Predementia Subjects with Cerebral Small Vessel Disease

Chong

Chai

et al. 2023

Biomolecules

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Tumor necrosis factor-receptor 1 (TNF-R1)-mediated signaling is critical to the regulation of inflammatory responses. TNF-R1 can be proteolytically released into systemic blood circulation in a soluble form (sTNF-R1), where it binds to circulating TNF and functions to attenuate TNF-mediated inflammation. Increases of peripheral sTNF-R1 have been reported in both Alzheimer’s disease (AD) dementia and vascular dementia (VaD). However, the status of sTNF-R1 in predementia subjects (cognitive impairment, no dementia, CIND) is unknown, and putative associations with cerebral small vessel disease (CSVD), as well as with longitudinal changes in cognitive functions are unclear. We measured baseline serum sTNF-R1 in a longitudinally assessed cohort of 93 controls and 103 CIND, along with neuropsychological evaluations and neuroimaging assessments. Serum sTNF-R1 levels were increased in CIND compared with controls (p < 0.001). Higher baseline sTNF-R1 levels were specifically associated with lacunar infarcts (rate ratio = 6.91, 95% CI 3.19–14.96, p < 0.001), as well as lower rates of cognitive decline in the CIND subgroup. Our data suggest that sTNF-R1 interacts with vascular cognitive impairment in a complex manner at predementia stages, with elevated levels associated with more severe CSVD at baseline, but which may subsequently be protective against cognitive decline.

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Melatonin: Therapeutic Intervention in Mild Cognitive Impairment and Alzheimer Disease

Cited by 9 publications

References 31 publications

Melatonin and Major Neurocognitive Disorders: Beyond the Management of Sleep and Circadian Rhythm Dysfunction

Melatonin and Major Neurocognitive Disorders: Beyond the Management of Sleep and Circadian Rhythm Dysfunction

Molecular Hybridization as a Tool in the Design of Multi-target Directed Drug Candidates for Neurodegenerative Diseases

Elevated Soluble TNF-Receptor 1 in the Serum of Predementia Subjects with Cerebral Small Vessel Disease

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